changes in protein profiles in bortezomib applied multiple myeloma ...

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DNA as the first cell does. Therefore, if mutation is not repaired properly and before replication occurs, the mutated cells amplify to generate billions of cells that constitute a cancer (King and Robins, 2006; Lieberman and Marks, 2009). Figure 1.1. Loss of Normal Growth Control Carcinogenesis, the process by which cancers are developed, is a multistage mechanism resulting from the accumulation of errors in vital regulatory pathways. It is initiated in a single cell, which then multiplies and obtains additional alterations that give it a survival advantage over its neighbours (Figure 1.2) (King and Robins, 2006). Figure 1.2 represents development of cancer. Each connecting arrow refers several events and many pathways can exist between each stage. First step (Initiation) explains the generation of mutated cells in consequence of mutations. Following step (Promotion) expresses the proliferation of differentiated cells. Step three (Progression) states the formation of cancer. Subsequent to this uncontrolled growth, cancer cells that alter morphological properties, invade other tissues and metastasize. 3
Figure 1.2. Development of Cancer Six considerable characteristics found in cancer cells are called hallmarks of cancer (Hanahan and Weinberg, 2000). They are as follows : Self-sufficiency in growth signals, Insensitivity to antigrowth signals, Evasion of apoptosis, Limitless replicative potential, Sustained angiogenesis, Tissue invasion and metastasis. 1.2. Multiple Myeloma (MM) Multiple Myeloma (MM) (also known as myelomatosis, plasma cell myeloma or Kahler's disease) is a malignant B-cell neoplasm that is characterized by the accumulation of malignant plasma cells in the bone marrow. It is known as bone marrow cancer in the society and it is the second most common hematological disorder (Raab et al., 2009). It accounts for 2% of cancer deaths among the most dangerous cancer types (Zaidi and Vesole, 2001). Recently, increasing number of people is being diagnosed as MM. It has a yearly incidence of nearly 14-15 thousand that accounts for approximately 10% of all hematologic cancers in the US (San et al., 1999; Collins, 4
Page 1 and 2: CHANGES IN PROTEIN PROFILES IN BORT
Page 3 and 4: ACKNOWLEDGEMENTS First of all, with
Page 5 and 6: ÖZET BORTEZOMĠB UYGULANAN MULTĠP
Page 7 and 8: 2.1.4.1.2. Two-Dimensional Gel Elec
Page 9 and 10: LIST OF FIGURES Figure Page Figure
Page 11 and 12: LIST OF TABLES Table Page Table 1.1
Page 13: When normal cells in the body begin
Page 17 and 18: the myeloma cells does not help fig
Page 19 and 20: A rare form of MM called Nonsecreto
Page 21 and 22: 1.2.3. Risk Factors for MM A risk f
Page 23 and 24: of the mineralizations by adjusting
Page 25 and 26: To measure the levels of red cells,
Page 27 and 28: The levels of blood urea nitrogen (
Page 29 and 30: By using the system introduced by D
Page 31 and 32: 1.2.7.2. Biology of The Proteasome
Page 33 and 34: Figure 1.10. Ubiquitin-Proteasome P
Page 35 and 36: Figure 1.12. Effect of Bortezomib o
Page 37 and 38: encompasses the investigation of pr
Page 39 and 40: of modification. Ubiquitin is a sma
Page 41 and 42: the given cells. On the other hand,
Page 43 and 44: is-acrylamide (N,N'-methylene-bisac
Page 45 and 46: 2.1.4.2. Detection of Protein Spots
Page 47 and 48: ange of 600-2500 Da. This is the id
Page 49 and 50: ions resolved by the mass analyzer
Page 51 and 52: 2.1.4.5.2. Mass Analyzers Figure 2.
Page 53 and 54: There is no doubt that different ma
Page 55 and 56: mask low-quantity proteins that may
Page 57 and 58: 3.1. Materials 3.1.1. Medias CHAPTE
Page 59 and 60: 3.2.5. Cell Proliferation Assay Ant
Page 61 and 62: After 72 hour incubation period at
Page 63 and 64: eceptors of the Tumor Necrosis Fact
Page 65 and 66:
The preparation of stock BSA Standa
Page 67 and 68:
3.2.6.3. Detection of the Loss of M
Page 69 and 70:
centrifugation, the supernatant was
Page 71 and 72:
selected symmetrically to load the
Page 73 and 74:
approximately 35 ml, the volume of
Page 75 and 76:
After electrophoresis was finished,
Page 77 and 78:
7 Day Two: Reduction, Alkylation, a
Page 79 and 80:
CHAPTER 4 RESULTS AND DISCUSSION 4.
Page 81 and 82:
% Changes in Cytoplasmic/Mitochondr
Page 83 and 84:
Table 4.1. Magnified Segments of Di
Page 85 and 86:
Table 4.1. Magnified Segments of Di
Page 87 and 88:
After labeling, black and red color
Page 89 and 90:
78 7 8 Y2S Y3S Table 4.2. Results o
Page 91 and 92:
80 12 S4Ca Table 4.2. Results of Di
Page 93 and 94:
82 27 Y5S Table 4.2. Results of Dif
Page 95 and 96:
Spot 4, Ubiquitin-conjugating enzym
Page 97 and 98:
is a transcriptional repressor, but
Page 99 and 100:
activity and loss of mitochondrial
Page 101 and 102:
distributed, but correlate with nat
Page 103 and 104:
DeMartino, G. N. and Slaughter, C.
Page 105 and 106:
proteomic analyses of a systematica
Page 107 and 108:
Mahindraa, A., Hideshimab, T. and A
Page 109 and 110:
Richardson, P. G., Hideshima, T. an
Page 111 and 112:
Terpos, E. 2008. Bortezomib Directl
Page 113 and 114:
A.1. RPMI-1640 Growth Medium APPEND
Page 115 and 116:
Table B.1. Chemicals and Reagents U
Page 117 and 118:
B.4.3. Standard Curve for BSA Table
Page 119 and 120:
Urea (8M) 4.8 g CHAPS (%2) 0.2 g DT
Page 121 and 122:
E. F. G. STOCK REAGENT PREPARATION
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